Background: Liver transplantation is the most durable treatment option for ESLD. Due to acute shortage of cadaveric organs Living donor liver transplantation has gained momentum especially in Asian countries. Size of the liver graft or the remnant liver is often expressed as a percentage of the standard liver volume (SLV) of the patient. Various formulas for SLV have been derived but only Chandramohan formula is derived for Indian population. Our aim was to carry out a study to validate the Indian formula based on the actual liver volumes (ALV) that we got from the cadaveric donor livers.
Material and methods: This prospective study included 33-brain dead cadaveric donor of either sex. Body surface area was calculated by Mosteller's formula. Graft weight was measured after the bench surgery. Standard liver volume was calculated by formula derived by Chandramohan et al and compared with actual liver weight.
Result: Chandramohan formula underestimates actual liver weight in Indian population. With our data we derived a formula for standard liver volume for Indian population.
Conclusion: No accurate formula of SLV for Indian population. We attempted to derive a formula for SLV for Indian population. However our data is very limited needs larger cohort for proper estimation.

Small-for-size syndrome remains the greatest limiting factor for the expansion of liver transplantation (apart from cadaveric organ donation) and has been the major cause of worse short-term prognoses after LDLT. The size of the graft, ( GRWR < 0.8 or graft to SLV ratio <30–40%, portal hyperperfusion, obstructed hepatic venous drainage, MELD score, and graft steatosis may be responsible for the pathogenesis of SFSS. Sinusoidal shear stress may be the principal common pathway in the pathogenesis. Living donor grafts with portal pressure more than 20 mmHg or portal flow exceeding 250 mL/min per 100 g have a higher risk of graft failure. The role of decrease arterial flow in response to portal hyperflow remains to be elucidated. Acute portal hypertension and increased shear stress caused by a partial hepatectomy triggers the regeneration of the remaining liver, though liver dysfunction is seen to be due to sudden portal hypertension, microcirculatory ischemia, reduced oxygen delivery, and hepatocellular dysfunction. The differences in sinusoidal pressure, or differences in the hepatotropic substances delivered to the graft or the liver remnant may be the difference between grafts that survive and grafts that don't. We need to find the threshold level of hyperperfusion that does more harm than good.

Electron microscopic examination is often not considered an essential diagnostic modality for evaluation of renal transplant biopsies in patients with graft dysfunction. However, recent reports suggest that ultrastructural evaluation of renal graft biopsies from patients presenting with allograft dysfunction is required to diagnose early changes of chronic rejection. These early ultrastructural lesions involve both glomerular and interstitial peritubular renal capillaries. The routine ultrastructural examination of renal graft biopsies in patients with chronic graft dysfunction can reduce the non-specific diagnosis of interstitial fibrosis and tubular atrophy – not otherwise specified. Ultrastructural evaluation of renal graft biopsies from patients presenting with proteinuria is also important along with routine histology and immunofluorescence to diagnose recurrent or de novo glomerular conditions and differentiate them from transplant glomerulopathy. The definite role of electron microscope in acute rejection is still controversial. The limitations and various aspects of application of electron microscopy in the evaluation of renal graft biopsies are discussed. These include its application in the diagnosis of rejection, transplant glomerulopathy, infections and in recurrent and de novo glomerular diseases. Ancillary techniques including immunoelectron microscopy are also described.

We report a case of recurrent squamous cell carcinoma (SCC) of the skin in a post-renal transplant recipient occurring 5 years after transplantation. The purpose of reporting is not for its rarity or uniqueness, but to re-emphasize the fact that skin malignancies could be lethal. The SCC in our patient was aggressive, recurrent and metastasized early. It is worthy to reassert the need for annual dermatology screening to be made mandatory in transplant recipients to identify pre-malignant and early cancerous lesions.

The post-operative course after mesenteric revascularization for chronic mesenteric ischemia is associated with significant morbidity (5%–30%) and mortality (5%–12%), since many of these patients develop significant liver dysfunction, with cholestasis and transaminitis, and a vitamin-K resistant coagulopathy with a fall in platelet count. An elderly male underwent mesenteric revascularization and developed ascites, jaundice, transaminitis and coagulopathy with thrombocytopenia; which gradually recovered over 7–10 days. The post-operative findings are remarkably similar to that seen in portal hyperperfusion, or small for size syndrome (SFSS) after living donor liver transplantation. Mesenteric revascularization results in improved blood blow through the splanchnic circulation, and results in an increased portal blood flow after repair. The portal hyperperfusion may explain the manifestations seen after mesenteric revascularization, including the liver dysfunction, coagulopathy and in extreme cases renal and pulmonary dysfunction.